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REVIEW
Division of Molecular Cardiovascular Biology, Cincinnati Childrens Hospital Research Foundation, Cincinnati, Ohio
Jeff.Robbins{at}cchmc.org
Congenital heart defects affect ~1 in every 100 live births, and deficits in the formation of the mitral, tricuspid, and outflow tract valves account for 2025% of all cardiac malformations. Mutations in genes that affect Ras signaling have been identified in individuals with congenital valve disease associated with Noonan syndrome and neurofibromatosis type 1. Dissection of Ras-related signaling pathways during valvulogenesis provides seminal insight into cellular and molecular mechanisms that contribute to congenital heart disease.
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